Association of HSD17B13 rs72613567: TA allelic variant with liver disease: review and meta-analysis

Abstract

Background To assess the association of HSD17B13 rs72613567:TA allelic variant with liver disease, we performed the current review and meta-analysis. Methods Seven studies were identified by a search of CNKI,CBM,MEDLINE, PubMed, EMBASE, and CENTRAL databases from inception to November 2021. Odds ratios (ORs) with 95% confidence interval (CI) were calculated using random effects model or fixed effects model based on the between-study heterogeneity. The Stata 14.0 software was employed for data analysis. Results Statistical analysis showed that the HSD17B13 rs72613567:TA allelic variant can decrease the risk of hepatocellular carcinoma(HCC) in nonalcoholic fatty liver disease (NAFLD) patients, alcoholic fatty liver disease (ALD) patients and viral hepatitis patients (TA vs T OR = 0.766, 95% CI = 0.682–0.860, P = 0.000; TATA + TAT vs TT OR = 0.755, 95% CI = 0.645–0.885, P = 0.001) or healthy controls(TA vs T OR = 0.649, 95% CI = 0.431–0.977, P = 0.038). Besides, the HSD17B13 rs72613567:TA allelic variant can also provide protection from nonalcoholic fatty liver disease (NAFLD) not only in entire population (TA vs T OR = 0.669, 95% CI = 0.524–0.856, P = 0.001) but also in healthy people (TA vs T OR = 0.600, 95% CI = 0.464–0.777, P = 0.000). No significant publication bias found in this airticle. Conclusion The present findings suggest HSD17B13 rs72613567:TA allelic variant can reduce the risk of HCC and NAFLD in the entire population studied.

Risk Factors for Hepatocellular Carcinoma in Patients With Non-Alcoholic Fatty Liver Disease

“…This polymorphism was associated with reduced risk of alcoholic cirrhosis by 42% among heterozygotes and by 73% among homozygotes; the risk of NALFD-cirrhosis was reduced by 26% among heterozygotes and by 49% among homozygotes.98 It seems that HSD17B13 (86) . The most of data about ALD or NAFLD genetic polymorphisms showed the critical role of factors associated with lipid metabolism in the liver, from the early stages to HCC (86) .…”

“…A variant rs72613567: TA in HSD17B13, encoding the hepatic lipid droplet protein hydroxysteroid 17-beta dehydrogenase, modulates liver inflammation and fibrosis but does not have a significant role in lipid accumulation in the liver (86) . This polymorphism was associated with reduced risk of alcoholic cirrhosis by 42% among heterozygotes and by 73% among homozygotes; the risk of NALFD-cirrhosis was reduced by 26% among heterozygotes and by 49% among homozygotes.98 It seems that HSD17B13 (86) . The most of data about ALD or NAFLD genetic polymorphisms showed the critical role of factors associated with lipid metabolism in the liver, from the early stages to HCC (86) .…”

Advances in genetic variation in metabolism-related fatty liver disease

“…A genetic variant of HSD17B13 (rs72613567, T > TA) was first described in 2018 and was associated with a reduced risk of MAFLD ( Abul-Husn et al, 2018 ), other variants of HSD17B13 (rs6834314, A > G and rs9992651, G > A) were later associated with lower inflammatory scores in patients with MAFLD, which may be related to protection against MAFLD ( Motomura et al, 2021 ). A meta-analysis showed that a polymorphism of the HSD17B13rs72613567:TA allele variant was associated with a reduced risk of HCC and MAFLD in the entire study population ( Tang et al, 2021 ). Other studies have found that there may be interaction between HSD17B13 rs72613567 gene variation and PNPLA3 rs738409, which directly affect the expression level of PNPLA3 mRNA in liver and reduce the activity of PNPLA3 p. I148 ( Abul-Husn et al, 2018 ).…”

Metabolic-associated fatty liver disease from childhood to adulthood: State of art and future directions

“…Fatty liver pathophysiology includes a well-known spectrum of determinants such as inflammation, IR, genetics and environment[ 4 , 28 , 29 ]. Genetic determinants commonly implied in NAFLD susceptibility (such as PNPLA3 [ 30 - 32 ], TM6SF2 [ 33 ], MBOAT7 [ 34 - 36 ] and HSD17B13 [ 37 - 42 ] genes) have been also linked to MAFLD pathogenesis[ 43 - 45 ] (Table 2 ). In particular, the effect of the PNPLA3 I148M polymorphism as a key genetic factor for NAFLD susceptibility across different ethnicities has been largely recognized both in adults and children[ 45 ].…”